Early embryonic lethality in mice deficient in the p110β catalytic subunit of PI 3-kinase

Early embryonic lethality in mice deficient in the p110β catalytic subunit of PI 3-kinase Mammalian Genome 13, 169-172 (2002). DOI: 10.1007/s00335-001-2123-x Mammalian P41OIlle Incorporating ~louse Genome 9 Springer-Verlag New York Inc. 2002 Early embryonic lethality in mice deficient in the pll013 catalytic subunit of PI 3-kinase Lei Bi, Ichiro Okabe, David J. Bernard, Robert L. Nussbaum Genetic Diseases Research Branch, National Human Genome Research Institute, National Institutes of Health, 49 Convent Drive, 4A72, Bethesda, Maryland 20892-4472, USA Received: 27 August 2001 / Accepted: 31 October 2001 An important class of phosphorylated phosphoinositides carrying a of Pik3ca die in utero between E9.5 to El0.5 because of a prolif- phosphate group at the 3' position of the inositol ring are generated erative defect (Bi et al. 1999). This result implies that other iso- by phosphoinositide 3-kinases (PI 3-kinases) which convert forms including 13 cannot compensate for the function of the PtdIns, PtdIns(4)P, and PtdIns(4,5)P 2 to PtdIns(3)P, PtdIns(3,4)P2, isoform at this stage. Here we report the successful targeting of the and PtdIns(3,4,5)P 3 respectively (Frnman et al. 1998; Vanhaese- Pik3cb encoding the beta isoform of pll0, to create a partial broeck et al. 2001). The PI 3-kinases can be grouped into three deletion allele which, in the homozygous state, leads to very early classes according http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Mammalian Genome Springer Journals

Early embryonic lethality in mice deficient in the p110β catalytic subunit of PI 3-kinase

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Publisher
Springer-Verlag
Copyright
Copyright © 2002 by Springer-Verlag New York Inc
Subject
Life Sciences; Anatomy; Cell Biology; Zoology
ISSN
0938-8990
eISSN
1432-1777
D.O.I.
10.1007/BF02684023
Publisher site
See Article on Publisher Site

Abstract

Mammalian Genome 13, 169-172 (2002). DOI: 10.1007/s00335-001-2123-x Mammalian P41OIlle Incorporating ~louse Genome 9 Springer-Verlag New York Inc. 2002 Early embryonic lethality in mice deficient in the pll013 catalytic subunit of PI 3-kinase Lei Bi, Ichiro Okabe, David J. Bernard, Robert L. Nussbaum Genetic Diseases Research Branch, National Human Genome Research Institute, National Institutes of Health, 49 Convent Drive, 4A72, Bethesda, Maryland 20892-4472, USA Received: 27 August 2001 / Accepted: 31 October 2001 An important class of phosphorylated phosphoinositides carrying a of Pik3ca die in utero between E9.5 to El0.5 because of a prolif- phosphate group at the 3' position of the inositol ring are generated erative defect (Bi et al. 1999). This result implies that other iso- by phosphoinositide 3-kinases (PI 3-kinases) which convert forms including 13 cannot compensate for the function of the PtdIns, PtdIns(4)P, and PtdIns(4,5)P 2 to PtdIns(3)P, PtdIns(3,4)P2, isoform at this stage. Here we report the successful targeting of the and PtdIns(3,4,5)P 3 respectively (Frnman et al. 1998; Vanhaese- Pik3cb encoding the beta isoform of pll0, to create a partial broeck et al. 2001). The PI 3-kinases can be grouped into three deletion allele which, in the homozygous state, leads to very early classes according

Journal

Mammalian GenomeSpringer Journals

Published: Jul 31, 2007

References

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